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The pseudokinase Trib1 regulates the transition of exhausted T cells to a KLR CD8 effector state and its deletion improves checkpoint blockade. | LitMetric

AI Article Synopsis

Article Abstract

T cell exhaustion (T ) impairs the ability of T cells to clear chronic infection or cancer. While exhausted T cells are hypofunctional, some exhausted T cells retain effector gene signatures, a feature that is associated with expression of KLRs (killer lectin-like receptors). Although KLR T cells may improve control of chronic antigen, the signaling molecules regulating this population are poorly understood. Using scRNA-seq, flow cytometry, RNA velocity, and scTCR-seq, we demonstrate that deleting the pseudokinase Trib1 shifts T towards CX3CR1 intermediates (T ) with robust enrichment of KLR CD8 T cells (T ) via clonal T cell expansion. These changes are associated with globally increased KLR gene expression throughout the exhaustion program. Further, Trib1 loss augments anti-PD-L1 blockade to improve viral clearance by expanding the T population. Together, these data identify Trib1 as an important regulator of T cell exhaustion whose targeting enhances the KLR effector state and improves the response to checkpoint inhibitor therapy.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9948998PMC
http://dx.doi.org/10.1101/2023.02.16.528833DOI Listing

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